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Phenotypes Associated with This Genotype
Genotype
MGI:5906002
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Nr2f2)Tsa/Gt(ROSA)26Sor+
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (3 available); any A1cf mutation (6 available)
Gt(ROSA)26Sortm1(CAG-Nr2f2)Tsa mutation (0 available); any Gt(ROSA)26Sor mutation (502 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen-treated mice show increased mortality

cardiovascular system
• tamoxifen-treated mice develop greatly enlarged heart 16 days after induction
• tamoxifen-treated mice exhibit impaired cardiac fuel utilization
• tamoxifen-treated mice develop dilated cardiomyopathy, showing increased left ventricular interior dimension, reduced fractional shortening, and decreased relative wall thickness
• 16 days after induction with tamoxifen, mice exhibit contractile dysfunction analogous to end-stage dilated cardiomyopathy

cellular
• mitochondria exhibit increased distance between cristae in the heart 9 days after induction with tamoxifen
• mitochondria exhibit a round in the heart 9 days after induction with tamoxifen
• tamoxifen-treated hearts exhibit reduced glucose oxidation rates ex vivo
• tamoxifen-treated hearts exhibit a lower oleate oxidation rate ex vivo
• reduction of enzyme activities of complexes I, II, III, and IV is isolated mitochondria of ventricles from tamoxifen-treated mice
• mitochondrial protein function is compromised in hearts of tamoxifen-treated mice, with a reduction of mitochondrial aconitase activity
• however, the number and density of mitochondria are normal in hearts
• mitochondrial respiration rate is lower in heart 4 days after induction with tamoxifen when cardiac dysfunction is not yet observed
• higher levels of oxidized proteins are seen in heart mitochondria of day 9 of induction with tamoxifen
• decrease of mitochondrial oxygen consumption rate and lower mitochondrial ATP content in hearts of tamoxifen-treated mice, suggesting a reduction in oxidative phosphorylation capacity and ATP production in mitochondria

homeostasis/metabolism
• tamoxifen-treated hearts exhibit a lower oleate oxidation rate ex vivo
• tamoxifen-treated hearts show decreased oxygen consumption rate

muscle
• tamoxifen-treated mice develop dilated cardiomyopathy, showing increased left ventricular interior dimension, reduced fractional shortening, and decreased relative wall thickness
• 16 days after induction with tamoxifen, mice exhibit contractile dysfunction analogous to end-stage dilated cardiomyopathy

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
dilated cardiomyopathy DOID:12930 OMIM:PS115200
J:227012


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
10/08/2019
MGI 6.14
The Jackson Laboratory